ArticleMolecular cancer2024
JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Single-cell profiling of natural killer/T-cell lymphoma reveals stratified immune features and potential therapeutic implications.Nature communications · 2026Article
- TP53, HIF1A, and CDKN2A in Hepatocellular Carcinoma: Roles in Senescence, Ferroptosis, and Prognosis.Clinical and translational gastroenterology · 2026Article
- Basal cell subsets, as biomarker to predict the therapeutic effect of neoadjuvant therapy for esophageal carcinoma.Journal of cancer research and clinical oncology · 2026Article
- A unique transcriptomic landscape defines African-specific grade group 1 prostate cancer.Research square · 2026Article
- High altitude-mediated immune remodeling accelerates aging.Science advances · 2026Article
- STAT1/3/5 Functions Driving Lipid and Energy Metabolism in Cancer and Immunity.International journal of molecular sciences · 2026Review
- Senescence-related gene signature predicts prostate cancer progression and identifies PCNA as a therapeutic target via multi-omics machine learning integration.British journal of cancer · 2026Article
- Time-resolved multiomics profiling reveals chromatin O-GlcNAc modification promotes senescence-associated transcriptional program.Nature communications · 2026Article
- PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages.European journal of medical research · 2026Article
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- Bibliometric Insights into Aging and Immune Function in Prostate Cancer: Focus on Chronic Inflammation.Journal of inflammation research · 2026Review
- MAVS/CMTM6 axis couples mitochondrial homeostasis to immunogenic senescence via CCL3-driven T-cell recruitment in renal carcinoma.Journal for immunotherapy of cancer · 2025Article
- Persistent and Dose-Dependent Neural and Metabolic Gene Expression Changes Induced by Transient Citalopram Exposure in Zebrafish Embryos.International journal of molecular sciences · 2025Article
- Targeting the ROS-ferroptosis-inflammation cycle with a nanozyme-functionalized hydrogel for intervertebral disc repair.Nature communications · 2025Article
- Spatial Transcriptional Dynamics of CD74⁺ B Cells in Tertiary Lymphoid Structures Drive Immune Evolution in Penile Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- The AP-1 factor JUNB correlates with poor survival of patients with esophageal adenocarcinoma.Scientific reports · 2025Article
- Multi-omics dissection of MAPK-driven senescence unveils therapeutic vulnerabilities in KIAA1549::BRAF-fusion pediatric low-grade glioma models.Signal transduction and targeted therapy · 2025Article
- Transient intracellular expression of PD-L1 and VEGFR2 bispecific nanobody in cancer cells inspires long-term T cell activation and infiltration to combat tumor and inhibit cancer metastasis.Molecular cancer · 2025Article
- Cellular senescence offers distinct immunological vulnerabilities in cancer.Trends in cancer · 2025Review
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34 authors.
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Abstract
backgroundProstate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated as potential oncogenic drivers, the molecular programs contributing to prostate cancer progression are not fully understood.
methodsWe analyzed JUN expression in clinical prostate cancer samples across different stages and investigated its functional role in a Pten-deficient mouse model. We performed histopathological examinations, transcriptomic analyses and explored the senescence-associated secretory phenotype in the tumor microenvironment.
resultsElevated JUN levels characterized early-stage prostate cancer and predicted improved survival in human and murine samples. Immune-phenotyping of Pten-deficient prostates revealed high accumulation of tumor-infiltrating leukocytes, particularly innate immune cells, neutrophils and macrophages as well as high levels of STAT3 activation and IL-1β production. Jun depletion in a Pten-deficient background prevented immune cell attraction which was accompanied by significant reduction of active STAT3 and IL-1β and accelerated prostate tumor growth. Comparative transcriptome profiling of prostate epithelial cells revealed a senescence-associated gene signature, upregulation of pro-inflammatory processes involved in immune cell attraction and of chemokines such as IL-1β, TNF-α, CCL3 and CCL8 in Pten-deficient prostates. Strikingly, JUN depletion reversed both the senescence-associated secretory phenotype and senescence-associated immune cell infiltration but had no impact on cell cycle arrest. As a result, JUN depletion in Pten-deficient prostates interfered with the senescence-associated immune clearance and accelerated tumor growth.
conclusionsOur results suggest that JUN acts as tumor-suppressor and decelerates the progression of prostate cancer by transcriptional regulation of senescence- and inflammation-associated genes. This study opens avenues for novel treatment strategies that could impede disease progression and improve patient outcomes.
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